沙丁胺醇喷雾剂对致敏豚鼠和大鼠气管平滑肌痉挛的显效关系研究

目的:研究沙丁胺醇喷雾剂对过敏性支气管平滑肌痉挛的缓解作用。方法:采用离体气管法和肺溢流法观察沙丁胺醇喷雾剂对致敏豚鼠和大鼠的支气管平滑肌痉挛的缓解作用,采用整体动物药物引喘法观察沙丁胺醇喷雾剂对致敏豚鼠过敏性哮喘保护作用。结果:沙丁胺醇10-6molL、3×10-6molL、10-5molL剂量下,对致敏豚鼠离体气管平滑肌收缩有抑制作用;0.2mgkg、0.4mgkg、0.8mgkg沙丁胺醇对致敏麻醉大鼠肺溢流量具有抑制作用;该剂量下沙丁胺醇对致敏豚鼠过敏性哮喘有保护作用,均产生显著性差异。结论:沙丁胺醇喷雾剂对致敏豚鼠离体气管平滑肌有松弛作用,明显延长组织胺与乙酰胆碱致敏豚鼠引喘潜伏期,减少致敏麻醉大鼠的肺溢流量。     

硫酸寡糖对豚鼠气管平滑肌的作用

目的 观察硫酸寡糖对组胺(His)、乙酰胆碱(Ach)引起的正常豚鼠离体气管平滑肌收缩的影响、对卵白蛋白(OVA)致敏豚鼠离体气管平滑肌受到OVA攻击时引起收缩的影响及对吸入His引起的正常整体豚鼠哮喘的影响。方法 采用豚鼠离体气管片法、致敏豚鼠离体气管Schultz-Dale法和整体动物引喘法。结果 硫酸寡糖能显著抑制His引起的正常豚鼠离体气管平滑肌收缩,但对Ach引起的正常豚鼠离体气管平滑肌收缩无显著抑制作用;能显著抑制OVA诱发的致敏豚鼠离体气管平滑肌的收缩;能显著延长His引喘潜伏期,使抽搐动物数减少。结论 硫酸寡糖具有抗His、抗过敏和平喘作用。     

速效止咳糖浆平喘作用的研究

目的研究速效止咳糖浆的平喘作用。方法采用整体动物引喘试验和离体豚鼠螺旋条作为实验对象,观察速效止咳糖浆对整体动物药物引喘的保护作用及3种致痉剂引起支气管收缩的影响。结果速效止咳糖浆对组胺-乙酰胆碱诱发的喘息有保护作用,表现为明显抑制哮喘反应,引喘潜伏期明显延长;对豚鼠离体气管平滑肌的静息张力无明显影响,但对乙酰胆碱、组胺、氯化钾所致的收缩有抑制作用,但均有剂量依赖性。小鼠口服LD 50>200 g生物/kg。结论速效止咳糖浆具有平喘作用,且毒性较小。     

速效止咳糖浆平喘作用的研究

目的 研究速效止咳糖浆的平喘作用.方法 采用整体动物引喘试验和离体豚鼠螺旋条作为实验对象,观察速效止咳糖浆对整体动物药物引喘的保护作用及3种致痉剂引起支气管收缩的影响.结果 速效止咳糖浆对组胺-乙酰胆碱诱发的喘息有保护作用,表现为明显抑制哮喘反应,引喘潜伏期明显延长;对豚鼠离体气管平滑肌的静息张力无明显影响,但对乙酰胆碱、组胺、氯化钾所致的收缩有抑制作用,但均有剂量依赖性.小鼠口服LD 50＞200 g生物/kg.结论 速效止咳糖浆具有平喘作用,且毒性较小.     

菊胡肺宁流浸膏对动物呼吸系统的药理作用

系统地研究了菊胡肺宁流浸膏对动物呼吸系统的药理作用。结果表明，菊胡肺宁流浸膏能明显抑制氨气所致小鼠咳嗽，显著增加小鼠气管内苯酚红分泌量，促进蟾蜍口腔粘膜纤毛运动，松弛豚鼠离体气管平滑肌，拮抗组织胺对豚鼠离体气管平滑肌的收缩作用，并可抑制乙酰胆碱和组织胺喷雾引起的豚鼠哮喘，使引喘潜伏期明显延长。     

气管炎丸的药理学研究

目的:研究气管炎丸的止咳、平喘、祛痰作用。方法:采用豚鼠离体气管法和拘橼酸引喘法观察气管炎丸的平喘作用;用雾化氨水刺激小鼠引咳法观察该药的镇咳作用;用小鼠酚红实验观察其祛痰作用。结果:该药可以有效地降低动物由氨水刺激引咳的咳嗽次数,可以明显延长豚鼠致喘的潜伏期,对乙酰胆碱及组胺造成的豚鼠离体气管平滑肌收缩有显著的拮抗作用,可以增加小鼠气管及支气管酚红的分泌量。结论:气管炎丸具有较好的止咳、平喘、祛痰效果。     

清肺消炎丸对豚鼠的镇咳平喘作用研究

目的：研究清肺消炎丸对豚鼠的镇咳平喘作用。方法：采用枸橼酸诱发豚鼠咳嗽模型,记录引咳后3min内的咳嗽次数,观察清肺消炎丸的镇咳作用。采用豚鼠离体气管平滑肌收缩实验和组胺引喘的活体动物实验对清肺消炎丸的平喘作用进行评价。离体实验中测定药物对乙酰胆碱引起的气管平滑肌收缩的收缩曲线,计算收缩百分率;整体动物实验中测定给药后豚鼠的延喘时间用来表征药物平喘作用的强弱。结果：清肺消炎丸能有效减少豚鼠的咳嗽次数,显著延长咳嗽潜伏期;对豚鼠离体气管收缩的抑制效果较好：对组胺致喘豚鼠的哮喘潜伏期有明显的延长作用。结论：清肺消炎丸具有良好的镇咳、平喘药理活性,为药物的临床应用和进一步开发提供了依据。     

鹅不食草挥发油平喘作用的实验研究

目的 研究鹅不食草挥发油的平喘作用。方法 应用氯乙酰胆碱和磷酸组胺进行药物性引喘以及离体豚鼠气管条的实验方法。结果 鹅不食草挥发油经口服给药可对抗氯乙酰胆碱和磷酸组胺引起的豚鼠喘息,明显延长豚鼠引喘潜伏期;鹅不食草挥发油还显著抑制磷酸组胺引起的豚鼠离体气管平滑肌的收缩。结论 鹅不食草挥发油有良好的平喘解痉作用。     

鹅不食草挥发油平喘作用的实验研究

目的研究鹅不食草挥发油的平喘作用。方法应用氯乙酰胆碱和磷酸组胺进行药物性引喘以及离体豚鼠气管条的实验方法。结果鹅不食草挥发油经口服给药可对抗氯乙酰胆碱和磷酸组胺引起的豚鼠喘息,明显延长豚鼠引喘潜伏期;鹅不食草挥发油还显著抑制磷酸组胺引起的豚鼠离体气管平滑肌的收缩。结论鹅不食草挥发油有良好的平喘解痉作用。     

肺必清片药效学实验研究

目的：为临床合理使用肺必清片治疗咳嗽、咳痰、哮喘等呼吸系统疾病提供可靠的实验依据。方法：采用整体动物实验法与离体气管法。结果：肺必清可显著减少氨水所致小鼠的咳嗽次数;显著增加大鼠气管的痰液引流量和小鼠气道腔的酚红排出量;显著延长组织胺与氯化乙酰胆碱对豚鼠引喘的潜伏期;明显地对抗组织胺与乙酰胆碱所致的豚鼠离体气管收缩,松弛气管平滑肌。结论：肺必清具有显著的镇咳、祛痰、平喘作用。     

神经生长因子抗体对哮喘模型大鼠肺中趋化素样因子1表达的影响

目的观察神经生长因子(NGF)抗体对OVA诱导的哮喘模型大鼠肺中趋化因子CKLF1的表达变化。方法采用OVA诱导的大鼠哮喘模型,通过腹腔给予NGF(8 ng.kg-1)及NGF抗体(0.1 mg.L-1),采用Western blot、ELISA和免疫组化观察CKLF1在支气管肺泡灌洗液(BALF)及肺组织中的表达变化。结果 CKLF1在OVA诱导的哮喘模型大鼠肺组织中的蛋白表达升高(P<0.05);NGF抗体能够降低CKLF1的表达;CKLF1在哮喘大鼠BALF中的含量升高(P<0.05),NGF抗体能够降低BALF中CKLF1的含量(P<0.05);NGF对肺组织及BALF中CKLF1的表达没有明显的影响。结论 NGF抗体能够抑制哮喘模型大鼠肺组织及支气管肺泡灌洗液中CKLF1的表达和释放,改善哮喘症状。     

Alpinia katsumadai seed extract attenuate oxidative stress and asthmatic activity in a mouse model of allergic asthma

Allergic asthma is a chronic inflammatory disorder of the airways characterized by biphasic airway obstruction. Oxidative stress plays an important role in the development of asthmatic conditions. Thus, identification of oxidative stress markers in bronchoalveolar lavage fluid (BALF) and lung tissue from ovalbumin (OVA)-sensitized mice could provide new insights into both the pathogenesis of the disease and the possible use of anti-oxidants to alleviate disease severity.     

贴敷"咳喘宁"贴膏对支气管哮喘模型大鼠肺泡灌洗液中炎性细胞的影响

目的:通过建立大鼠支气管哮喘模型,观察穴位贴敷“咳喘宁”贴膏对支气管哮喘模型大鼠肺泡灌洗液中炎性细胞的影响。方法:将60只Wistar大鼠按随机数字表分组法随机分为空白对照组(A组)、模型对照组(B组)、内服“桂龙咳喘宁”对照组(C组)、内服“地塞米松”对照组(D组)、穴位贴敷“咳喘宁”高剂量治疗组(E组)、穴位贴敷“咳喘宁”低剂量治疗组(F组)6组,每组10只。各组大鼠用Elwood法造模。于诱喘前10h开始给药,并分别观察各组哮喘模型大鼠肺泡灌洗液(BALF)中炎性细胞的改变。结果:与C组比较,D、E、F组炎性细胞减少有显著性差异(P<0.05);与D组比较,C组、E组、F组嗜酸性粒细胞明显增高,有显著性差异(P<0.05);各治疗组中的中性粒细胞都明显减少,与B组比较有显著性差异(P<0.05);各治疗组中淋巴细胞水平明显降低,P<0.05或P<0.01。结论:穴位贴敷“咳喘宁”贴膏对支气管哮喘模型大鼠有明显的抑制炎症的作用,其作用虽不及内服“地塞米松”组,但等同内服“桂龙咳喘宁”组;有明显的改善变态反应和增加免疫功能作用。     

Effects of astragaloside IV on IFN-gamma level and prolonged airway dysfunction in a murine model of chronic asthma

Astragaloside IV (AST) is the main active constituent of Radix Astragali, a Chinese herb traditionally used to prevent asthma attack from chronic asthma patients. Its efficacy and action mechanisms in asthma attack prevention remain nonetheless to be further explored. In this study, chronic asthma was induced exposing ovalbumin (OVA) sensitized mice to repeated OVA challenges twice every two weeks for 12 weeks. Mice were treated with AST for 4 weeks just after the final challenge. In this murine model of chronic asthma, the airway dysfunction and remodeling remained severe and was accompanied with suppression of the IFN-gamma level in the bronchoalveolar lavage fluid (BALF) even four weeks after the final challenge, indicating that the airway structural changes continued to develop even after interruption of OVA challenges. However, after AST treatment, the airway hyperresponsiveness was sharply relieved, accompanied by the reduction of collagen deposition and mucus production, meanwhile the inflammatory cells were decreased but the IFN-gamma level increased in BALF. In conclusion, AST could prevent the development of chronic asthma, thus reducing asthma attacks. Our results indicated that it should be used as a supplementary therapy on preventing asthma attacks from chronic asthma patients.     

Interference of a neutrophil recruitment inhibitory factor upon the accumulation of inflammatory cells and airway hyperreactivity in sensitized guinea-pigs after intranasal antigen challenge.

1. A neutrophil recruitment inhibitory factor (NRIF) recovered from the crude supernatant of lipopolysaccharide (LPS)-stimulated macrophages inhibited neutrophil migration following both intratracheal and intravenous administration of LPS, but did not alter the pattern of leukopenia/leucocytosis induced by intravenous LPS. 2. The correlation between airway infiltration by inflammatory cells and hyperreactivity in lungs from actively sensitized and challenged guinea-pigs was investigated by use of NRIF. 3. Increased eosinophil counts were found in the bronchoalveolar lavage fluid from guinea-pigs sensitized with 10 micrograms ovalbumin and challenged at day 14 by the intranasal administration of the antigen. The increase was evident 5 h after challenge and persisted at 24 h. Neutrophil numbers were also increased at this time. Pretreatment with NRIF suppressed the leucocyte increase in the bronchoalveolar lavage fluid. 4. Bronchoconstriction and histamine release induced by 3 ng PAF injected into the isolated lungs were increased in challenged guinea-pigs as compared to sensitized but unchallenged controls. Pretreatment of the animals with NRIF did not interfere with this response, but significantly reduced the bronchoconstriction induced by ovalbumin injection. 5. Even though the increased number of inflammatory cells in bronchoalveolar lavage and airway hyperresponsiveness were concomitant, NRIF inhibited cellular infiltration but failed to alter airway hyperreactivity to PAF, demonstrating that these events may occur independently. Conversely, the inhibition of antigen-induced bronchoconstriction by NRIF suggests that this response is dependent upon the emigration of granulocytes.     

The effects of (±)-Praeruptorin A on airway inflammation,remodeling and transforming growth factor-β1/Smad signaling pathway in a murine model of allergic asthma

(±)-Praeruptorin A (PA) is a pair of coumarin enantiomers isolated from the root of Peucedanum praeruptorum Dunn (PPD), a common Chinese herbal medicine for the treatment of asthma. Considering its anti-inflammatory, anti-contractile and anti-hyperplasia activities, the effects of PA on airway inflammation and airway remodeling were investigated using a murine model of chronic asthma. Ovalbumin-sensitized BALB/c mice were challenged with ovalbumin to induce asthma every other day on eight successive weeks. PA was administered intragastrically before every ovalbumin challenge. Airway responsiveness was evaluated by a lung function analysis system 48 h after the last ovalbumin challenge. The total and differential leukocytes in bronchoalveolar lavage fluid (BALF) were counted using a hemocytometer and Diff-Quick-stained smears. Lung tissue samples were used for hematoxylin and eosin, periodic acid Schiff, Masson's trichrome and α-SMA immunohistochemistry staining. Levels of cytokines in BALF, immunoglobulin (Ig) E in serum as well as expression of TGF-β1 and Smad proteins in lung tissue were measured by enzyme-linked immunosorbent assay, immunohistochemistry or western blot analysis. Compared with the model group, PA suppressed airway inflammation, airway hyperresponsive and remodeling, reduced levels of IL-4 and IL-13 in BALF, and IgE in serum, inhibited expression of TGF-β1 and pSmad2/3, up-regulated the expression of Smad7 in lung tissue, and also increased the levels of INF-γ in BALF. These results suggested that PA significantly suppressed airway inflammation and airway remodeling induced by ovalbumin challenge, and is a potential candidate for the treatment of asthma.     

Flt3 ligand: a novel cytokine prevents allergic asthma in a mouse model

Flt-3 ligand (FL), a recently described growth factor affecting early hematopoietic progenitor cells, can also support the expansion of dendritic cells secreting IL-12. Since type 2 T cells predominate in asthma and IL-12 prevents the differentiation of naive T lymphocytes to a type 2 phenotype, we hypothesized that FL could prevent the development of asthma-like conditions in the ovalbumin mouse model. We found that co-administration of FL during ovalbumin sensitization abrogated late allergic responses, but had no effect on early allergic responses. Airway hyperresponsiveness to methacholine was also blocked by FL treatment. Analysis of bronchoalveolar lavage (BAL) fluid demonstrated a significant reduction in eosinophils, with concomitant decreases in IL-5 and increases in IFN-gamma levels. However, there was no change in BAL fluid IL-4 and serum IgE levels. These data suggest that FL treatment prevents ovalbumin-induced asthma in the mouse and may provide a useful adjuvant in the treatment of human asthma.